The sequence of cellular and hemodynamic changes of chronic pulmonary hypertension induced by hypoxia and other stimuli.

It has been suggested that the lung has only a narrow range of structural responses to injury. For example, long-term injury results in emphysema, fibrosis, and pulmonary hypertension. Clinical and experimental models of chronic pulmonary hypertension suggest that this disease can be triggered by a number of interventions and that the structural changes in the pulmonary arterial circulation may vary depending on the stimulus. This report briefly reviews the structural changes that accompany the development of pulmonary hypertension in hypoxia- and Crotalaria-induced pulmonary hypertension in the rat and in repeated endotoxemia and continuous air embolization in the sheep. The studies indicate that of the structural changes considered characteristic of chronic pulmonary hypertension, the reduction in peripheral arterial volume as reflected by a loss in number of barium-filled arteries, extension of muscle into smaller intra-acinar arteries than normal, and reduction in external diameter of intra-acinar arteries are the changes that contribute to the sustained rise in pulmonary artery pressure. Increased medial and adventitial thickness of the normally muscular arteries seem to be secondary changes to this disease. Because the severity and range of structural changes differ between the experimental models of pulmonary hypertension, the data suggest that the lung, particularly the pulmonary arterial circulation, may have a more complex response to injury than originally suspected.